Modulation of natural killer activity by 12-O-tetradecanoylphorbol-13-acetate and benzoyl peroxide in phorbol ester-sensitive (SENCAR) and resistant (B6C3F1) mice.
Modulation of natural killer activity by 12-O-tetradecanoylphorbol-13-acetate and benzoyl peroxide in phorbol ester-sensitive (SENCAR) and resistant (B6C3F1) mice.
复制标题
12-O-十四烷酰佛波醇-13-乙酸酯和过氧化苯甲酰对佛波酯敏感 (SENCAR) 和耐药 (B6C3F1) 小鼠自然杀伤活性的调节。
DOI：
10.1093/carcin/9.11.1943
复制
发表时间：
1988
期刊：
影响因子：
4.7
通讯作者：
Yim,GK
中科院分区：
文献类型：
--
作者：
Updyke,LW;Chuthaputti,A;Pfeifer,RW;Yim,GK
隔日以2、4和8 μg/小鼠局部应用12-O-四癸酰基佛波醇-13-乙酸酯（TPA）两周后，（总计7 ×）或10、20和40 mg/小鼠过氧苯甲酰（BZP），自然杀伤（NK）活性测定在当地（引流下背部区域的淋巴结）n和全身（脾）淋巴组织。SENCAR小鼠在两阶段化学诱导的致癌方案中对TPA的肿瘤诱导敏感，在局部暴露于TPA后，表现出脾脏中NK活性的抑制（淋巴结中无显著变化）和这些器官中细胞数量的显著剂量依赖性增加。B6 C3 F1（C57 BL/6 × C3 H Fl）小鼠报告对TPA诱导的促进具有抗性，表现出淋巴结/脾脏中NK活性显著增加，仅引流结中细胞数量增加。与C57 BL/6亲本品系不同，B6 C3 F1小鼠也报告对BZP促进具有抗性。值得注意的是，该实验室的研究表明，B6 C3 F1小鼠接受BZP给药后，脾脏中的NK活性增加，与TPA给药后观察到的一样。这些数据表明，暴露于肿瘤促进剂导致的NK活性的改变可能部分地解释了特定品系小鼠对肿瘤发展的抗性。在SENCAR和B6 C3 F1小鼠中，从TPA给药动物中分离的脾细胞悬液对植物血凝素（PHA）（一种T细胞凝集素）的胚细胞生成反应以剂量依赖性方式受到抑制; BZP对两种品系的脾细胞反应均无影响。局部应用TPA和BZP后，两种品系小鼠的淋巴结细胞对PHA的成母细胞反应均增强。因此，淋巴细胞对PHA反应性的改变似乎与报告的SENCAR和B6 C3 F1小鼠对肿瘤促进的敏感性无关。
Following two weeks of topical application of 12-O-tetra-decanoylphorbol-13-acetate(TPA) at 2, 4 and 8 μg/mouse on alternate days (7 × total) or benzoyl peroxide (BZP) at 10, 20 and 40 mg/mouse, natural killer (NK) activity was determined in local (lymph nodes draining the lower dorsal region)n and systemic (spleen) lymphoid tissue in phorbol ester-sensitive (SENCAR) and resistant (B6C3F1) mice. SENCAR mice, sensitive to tumor induction by TPA in two-stage chemical-induced carcinogenesis protocols, demonstrated suppression of NK activity in the spleen (no significant change in lymph nodes) and substantial dose-dependent increases in cell numbers in these organs after topical exposure to TPA. B6C3F1 (C57BL/6 × C3H Fl) mice, reported to be resistant to TPA-induced promotion, demonstrated significant increases in NK activity in lymph nodes/spleen with an increase in cell numbers in the draining nodes only. Unlike the C57BL/6 parental Strain, B6C3F1 mice are also reported to be resistant to promotion with BZP. Significantly, studies in this laboratory indicated that B6C3F1 mice dosed with BZP demonstrated increased NK activity in the spleen as was observed after dosing with TPA. These data suggest that alterations in NK activity as a result of exposure to tumor promoters may, in part, account for the resistance of particular strains of mice to tumor development. In both SENCAR and B6C3F1 mice, the blastogenic response of spleen cell suspensions isolated from TPA-dosed animals to phytohemagglutinin (PHA), a T cell lectin, was suppressed in a dose-dependent manner; BZP had no effect on spleen cell responses in either strain. Blastogenic responses of lymph node cells to PHA were enhanced in both strains of mice after topical application of TPA and BZP. Therefore, alterations in lymphoid cell responsiveness to PHA appeared unrelated to the reported sensitivities of SENCAR and B6C3F1 mice to tumor promotion.